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Thrombolytic Therapy for Acute Stroke pp 43–62Cite as

The Ischemic Penumbra and Neuronal Salvage

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Part of the book series: Current Clinical Neurology ((CCNEU))

Abstract

The majority of focal cerebral ischemic events result from arterial occlusion caused by embolism or in situ thrombosis. This interruption in blood flow, if severe and prolonged, leads to cerebral infarction. Brain infarction results from a disruption in blood flow, which causes a reduction in oxygen and glucose supplied to the tissue. Glucose and oxygen deprivation causes a metabolic shift toward the production of lactic acidic. Coincident with this impairment of the Na+/Ca++ exchange pump, excessive glutamate release causes an unregulated amount of calcium to enter the cells. Intracellular calcium increases trigger a variety of processes that result in the breakdown of membranes and nucleic acids. In addition, the release of free radicals, the breakdown of the blood-brain barrier and development of the inflammatory response all work together to promote further cellular injury.

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  1. UCSD Stroke Center, University of California, San Diego

    Patrick Lyden MD

  2. Veteran’s Affairs Medical Center, San Diego, CA

    Patrick Lyden MD

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  1. USCD Stroke Center, University of California, San Diego

    Patrick D. Lyden MD

  2. Veteran’s Affairs Medical Center, San Diego, CA

    Patrick D. Lyden MD

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Lyden, P. (2005). The Ischemic Penumbra and Neuronal Salvage. In: Lyden, P.D. (eds) Thrombolytic Therapy for Acute Stroke. Current Clinical Neurology. Humana Press. https://doi.org/10.1385/1-59259-933-8:43

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